Figure 1.

Analysis of motor coordination and abnormal postures in Epm2b^−/− mutant mice after treatment with sodium selenate. (A) Rotarod-based analysis of motor coordination in controls (n = 23) and Epm2b^−/− mice (n = 24), in Epm2b^−/− mice with selenate treatment for 4 weeks (n = 22), and in Epm2b^−/− mice with selenate treatment over 10 weeks (n = 15) (trials 1–4). The mean latencies (time to fall from the rotarod) were significantly lower for Epm2b^−/− mice than for controls. Sodium selenate treatment for 4 weeks in Epm2b^−/− mice slightly increased the latency period, whereas a longer treatment significantly improved performance. Student’s t-test was performed for statistical evaluation. (B) Percentage of animals showing normal posture (0), partially altered (1) or high abnormal (2) stereotypical clasping of the hind limbs upon tail suspension. The frequent hind-limb clasping of Epm2b^−/− mice improved progressively with sodium selenate treatment (n = 23 for wild-type, n = 24 for ML, n = 20 for ML + Sel [4 weeks], and n = 15 for ML + Sel [10 weeks] mouse groups). A chi-square test was performed for statistical analysis. *Indicates p < 0.05, **indicates p < 0.01, and ***indicates p < 0.001 when control mice were compared to Epm2b^−/− mice; #indicates p < 0.05 and ###indicates p < 0.001 when Epm2b^−/− mice were compared to Epm2b^−/− mice with selenate treatment for 10 weeks. ML, malin-deficient mouse; Sel, sodium selenate.